Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease is the leading cause of death in patients receiving dialysis. This is attributed in part to the shared risk factors of cardiovascular disease and end-stage renal disease. The risk factors for coronary artery disease include the classic cardiac risk factors of diabetes mellitus, hypertension, dyslipidemia, and smoking. Also in this population, hyperparathyroidism, hypoalbuminemia, hyperhomocysteinemia, elevated levels of apolipoprotein (a), and the type of dialysis membrane may play a role. Management begins with risk factor modification and medical therapy including aspirin, beta blockers, angiotensin converting enzyme (ACE) inhibitors, and lipid-lowering agents. Revascularization is often important, and coronary artery bypass grafting appears to be preferable to percutaneous transluminal coronary angioplasty. This is especially true for those with multivessel disease, impaired left ventricular function, severe symptoms, or ischemia. Congestive heart failure is another common problem in dialysis patients. The management includes correction of underlying abnormalities, optimal dialysis, and medical therapy. Data obtained from the general population indicate obvious benefits from ACE inhibitors and beta blockers, and these agents would be considered the therapies of choice. Erythropoetin is also an essential component of therapy, but the ideal hemoglobin concentration has yet to be determined. Peritoneal dialysis may be helpful in severe cases of heart failure. Pericarditis is seen in less than 10% of dialysis patients and is best diagnosed by clinical examination and echocardiography. Intensive dialysis is often the best initial therapy. Pericardiocentesis is reserved for the setting of pericardial tamponade, but a pericardial window is more definitive.
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PMID:Cardiac complications of end-stage renal disease. 1092 9

Several studies shortly after the advent of coronary artery bypass surgery reported early atherosclerosis in saphenous vein grafts, and an association between dyslipidemia and graft occlusion. Lipid-lowering therapy in a number of trials resulted in reduced progression of atherosclerosis in vein grafts and fewer subsequent revascularization procedures. Presently, however, only a few patients are treated and reach target lipid levels. Percutaneous coronary interventions permit rapid relief of symptoms and ischemia, and return to full activity levels, but may not reduce the risk of death or nonfatal myocardial infarction in patients with chronic stable coronary artery disease. Whether optimal medical therapy, including aggressive lipid control, could decrease the need for some of these procedures is the subject of ongoing debate and research. Despite successful coronary artery revascularization, subsequent ischemic events continue to occur, supporting the requirement for successful secondary prevention interventions. Ultimately, optimal care of revascularization patients should include maximizing lipid profiles.
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PMID:Raising high-density lipoprotein cholesterol and lowering low-density lipoprotein cholesterol as adjunctive therapy to coronary artery revascularization. 1137 53

Myocardial infarction is still one of the main causes of mortality and morbidity in Western countries. The advances made in the last 30 years have made it possible to reduce mortality significantly (which is currently below two digits) as well as morbidity. The subject of secondary prevention of myocardial infarction gains particular significance in this context since 10 to 15% of the patients who survive the hospital phase of myocardial infarction die during the first year following discharge and, of these deaths, half occur in the first three months. Therefore, it is necessary to make an early definition of the risk of another coronary event, that is, to make a risk stratification. This should occur throughout hospitalization and should be complete at the time of discharge, never beyond the first weeks of evolution. Bearing in mind the age, sex, coronary risk factors, ischemia persistence, the degree of left ventricular dysfunction and the presence of malignant disrhythmias, there are three risk levels: high; intermediate; and low. An overall approach to secondary prevention of infarction should take into account that, apart from the factors of such high prognostic value (Chapter II) assessed in the definition of risk groups, the measures to reduce reinfarction and sudden death (Chapter III) and the control of the risk factors for heart disease (Chapter IV) should also be considered. The principal late complications of infarction with significant prognostic influence are described in Chapter III: left ventricular dysfunction; rhythm disturbances and residual ischemia. The diagnostic criteria and therapeutic objectives are considered in each of the groups with relevance to consolidated advances according to the modern concept of evidence based medicine, according to international regulations. The grading of scientific evidence into three distinct categories (A, B and C), based on five levels of evidence classified from I to V, is presented accordingly in relation to the therapeutic proposals. Chapter III deals with a set of therapeutic interventions used in secondary prevention because they reduce reinfarction and sudden death: platelet antiaggregants; anticoagulants; Beta blockers; calcium channel blockers; antioxidants and nitrates. A concept of particular clinical significance is presented for each of these groups of drugs. The last part contains an eminently clinical overall review of the principal advances in coronary risk factor control, new therapeutic acquisitions in atherosclerotic disease with natural relevance to hypolipidemic agents and statins, which apart from controlling the plasmatic levels of cholesterol, also stabilize the atherosclerotic plaque and reduce acute coronary events significantly. Apart from dyslipidemia, the classic risk factors are: smoking; hypertension; obesity; diabetes and sedentary life. In each case, reference is made to the general measures and specific approaches, as well as the pharmacological therapy according to evidence based medicine. The recommended attitudes are pointed out. The role of cardiac rehabilitation and postmenopausal hormone replacement therapy are also discussed in the last part of these recommendations, in which the on-going controversy regarding hormone replacement therapy is pointed out in view of the results of more recent clinical trials.
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PMID:[Secondary prevention in acute myocardial infarction]. 1147 86

Aspirin has been used for more than 100 years, but its mechanisms of action have only been understood in the past 20 years. Aspirin interferes with arachidonic acid metabolism in platelets and endothelial cells and thereby reduces thromboxane A2 and prostacyclin. It also has other mechanisms of action, including anti-inflammatory roles, protection from oxidative stress, enhancement of fibrinolysis, and suppression of plasma coagulation and platelet-dependent inhibition of thrombin generation. It has been used for primary and secondary prevention of myocardial ischemia, and for primary and secondary prevention of cerebrovascular ischemia. We review the 5 pivotal studies relating to primary prevention for cardiovascular risk and the many studies relating to secondary prevention of myocardial ischemia. We also review the utility of aspirin in primary prevention of myocardial infarction and stroke. We conclude that aspirin is one of the most potent drugs ever discovered and that its effects extend well beyond those of cycloxoxygenase enzyme inhibition. Aspirin treatment does not preclude control of underlying and comorbid conditions such as diabetes mellitus, hypertension, and dyslipidemia. For most patients, a daily dose of 325 mg is optimal. Patients must understand the potential for gastrointestinal upset and hemorrhagic complications. The utility of aspirin is greater in coronary artery disease prevention than in cerebrovascular prevention.
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PMID:Aspirin in the prophylaxis of coronary artery disease. 1235 34

Type 2 diabetes mellitus substantially increases the lifetime risk of both developing and dying from heart failure. While this appears to be explained in part by the well-known association of diabetes with hypertension, dyslipidemia, and coronary atherosclerosis, additional pathophysiologic mechanisms linking type 2 diabetes and heart failure have recently been suggested. These include the potentially adverse effects of hyperglycemia on endothelial function and redox state, effects of excess circulating glucose and fatty acids on cardiomyocyte ultrastructure, intracellular signaling and gene expression, and the possibility that diabetes may impair recruitment of the myocardial insulin-responsive glucose transport system in response to ischemia. Because many of these putative pathophysiologic mechanisms should be amenable to normalization of the diabetic metabolic milieu, strategies designed to more carefully control circulating levels of glucose and fatty acids might conceivably delay or prevent the development of heart failure.
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PMID:Diabetes mellitus and heart failure. 1282 71

To investigate whether marked and sustained lipid-lowering in subjects with stable angina pectoris and dyslipidemia reduces exercise-induced myocardial ischemia, 17 subjects were treated with dose-adjusted atorvastatin over 1 year and underwent serial evaluation of exercise electrocardiographic ischemic parameters, serum biomarkers, and brachial artery endothelial function. Endothelial function improved progressively and C-reactive protein, P-selectin, and tissue plasminogen activator inhibitor levels decreased, but there was no decrease in exercise electrocardiographic ischemia.
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PMID:Effect of atorvastatin on exercise-induced myocardial ischemia in patients with stable angina pectoris. 1460 94

The prevalence of peripheral arterial disease (PAD) increases with age. PAD in elderly persons may be asymptomatic, may be associated with intermittent claudication, or may be associated with critical limb ischemia. Other atherosclerotic vascular disorders, especially coronary artery disease (CAD), may coexist with PAD. Elderly persons with PAD are at increased risk for all-cause mortality, cardiovascular mortality, and mortality from CAD. Modifiable risk factors should be treated in persons with PAD such as cessation of cigarette smoking and control of hypertension, dyslipidemia, and diabetes. Statins have been shown to reduce the incidence of intermittent claudication and to improve treadmill exercise duration until the onset of intermittent claudication in persons with PAD and hypercholesterolemia. Antiplatelet drugs such as aspirin or clopidogrel, especially clopidogrel, should be administered to all persons with PAD. Persons with PAD should be treated with angiotensin-converting enzyme inhibitors and also with beta blockers if CAD is present. Cilostazol should be given to persons with intermittent claudication to improve exercise capacity unless heart failure is present. Exercise rehabilitation programs improve exercise time until claudication. Indications for lower extremity angioplasty, preferably with stenting, or bypass surgery are 1) incapacitating claudication in persons interfering with work or lifestyle; 2) limb salvage in persons with limb-threatening ischemia as manifested by rest pain, nonhealing ulcers, and/or infection or gangrene; and 3) vasculogenic impotence. However, amputation should be performed if tissue loss has progressed beyond the point of salvage, if surgery is too risky, if life expectancy is very low, or if functional limitations obviate the benefit of limb salvage.
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PMID:Management of peripheral arterial disease of the lower extremities in elderly patients. 1499 33

This article discusses the factors that contribute most to systolic and diastolic heart failure (HF): ischemic heart disease, hypertension,obesity, diabetes, and nephropathy. Diabetes often follows the insulin resistance syndrome in which obesity and hypertension are combined with dyslipidemia, and obesity is likely causal. Diabetes and hypertension are common causes of nephropathy, which in turn is a common precursor to HF. Insulin resistance, obesity,dyslipidemia, diabetes, and hypertension are risk factors for atherosclerotic coronary disease and left ventricular ischemia. Each is also a risk factor for diastolic dysfunction.
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PMID:Lifestyle and dietary modification for prevention of heart failure. 1533 18

Thromboembolism is considered the inciting cause of many vascular disorders including acute coronary syndrome (ACS), ischemic stroke, pulmonary embolism (PE), deep vein thrombosis (DVT), and mesenteric ischemia. Adrenergia and inflammation are known to accompany these conditions, particularly among arterial thromboembolic disorders, but the teleologic basis of these associations remains poorly understood. We argue that thromboembolism may sometimes be the result, rather than the cause, of acute vascular events, and may be precipitated by underlying adrenergia. Thromboembolic events are most prone to occur during parts of the circadian, seasonal, lifespan, and reproductive cycles with sympathetic dominance, as well as during behavioral, exertional, physiologic, and iatrogenic activation of sympathetic stress. Molecular evidence suggests that adrenergia and inflammation can promote coagulation and lead to co-activation of the pathways. Acute vascular events that occur without angiographic evidence of occlusion suggest that some infarcts may be attributable to adrenergia alone. "Embolic" disorders may represent asynchronous systemic phenomena rather than clot migration. During acute thromboembolism, downstream tissue hypoxia can activate maladaptive self-propelling cycles of sympathetic bias, inflammation, and coagulation. The counterproductive co-activation of these pathways may reflect a maladaptive interlink forged during the primordial evolution of trauma physiology. Their rapid co-mobilization enables rapid control of hemorrhage, microbial defense, and perfusion maintenance during trauma, but the pathways may behave maladaptively in the setting of modern diseases where endothelial injury may be more often precipitated by smoking, diabetes, dyslipidemia, or hypertension. Sympathetic blockade is already employed in ACS, and beta-blockers are used as antihypertensives to prevent stroke. Our hypothesis suggests that the benefits of beta-blockers in stroke may be independent of antihypertensive effects, and that adrenergia may represent a target for managing all thromboembolic disorders, independent of anti-coagulative and thrombolytic therapies. Perhaps reducing adrenergia, rather than maintaining high cerebral perfusion pressure, may represent a counterintuitive strategy for treating stroke and for reducing reperfusion injury. Plausible mechanisms by which autonomic dysfunction may induce venous thrombosis are discussed, especially in those with baroreceptor dysfunction, immobilization, or dehydration. Unexplained hypercoagulability of cancer may also operate through tumor-induced adrenergia and inflammation.
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PMID:Can thromboembolism be the result, rather than the inciting cause, of acute vascular events such as stroke, pulmonary embolism, mesenteric ischemia, and venous thrombosis?: a maladaptation of the prehistoric trauma response. 1569 86

Peripheral arterial disease (PAD) may be asymptomatic, may be associated with intermittent claudication, or may be associated with critical limb ischemia. Coronary artery disease (CAD) and other atherosclerotic vascular disorders may coexist with PAD. Persons with PAD are at increased risk for all-cause mortality, cardiovascular mortality, and mortality from CAD. Modifiable risk factors such as cessation of cigarette smoking and control of dyslipidemia, hypertension, and diabetes should be treated. Statins reduce the incidence of intermittent claudication and improve exercise duration until the onset of intermittent claudication in persons with PAD and hypercholesterolemia. Antiplatelet drugs such as aspirin or clopidogrel, especially clopidogrel, and angiotensin-converting enzyme inhibitors should be given to all persons with PAD. beta-Blockers should be given if CAD is present. Exercise rehabilitation programs and cilostazol improve exercise time until intermittent claudication. Indications for lower-extremity angioplasty, preferably with stenting, or bypass surgery are 1) incapacitating claudication in persons interfering with work or lifestyle; 2) limb salvage in persons with limb-threatening ischemia as manifested by rest pain, nonhealing ulcers, and/or infection or gangrene; and 3) vasculogenic impotence. However, amputation should be performed if tissue loss has progressed beyond the point of salvage, if surgery is too risky, if life expectancy is very low, or if functional limitations diminish the benefit of limb salvage.
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PMID:Management of peripheral arterial disease. 1570 52


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